Role of nitric oxide in diabetic nephropathy

Prabhakar, Sharma

doi:10.1016/j.semnephrol.2004.04.005

Cited by 138 publications

(126 citation statements)

References 86 publications

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“…Taken together, although the telomeric part of the MHC III appears to be an interesting region in the context of DN, more detailed mapping and functional studies are warranted to clarify potential causality of the particular markers. NOS3 is a well-documented functional candidate for DN susceptibility because of the involvement of nitric oxide in DN pathogenesis [39,40]. One of the first indications that genes within chromosome 7q35 (including NOS3) could influence genetic susceptibility to DN came from the nonparametric linkage study in Pima Indians [16].…”

Section: Discussionmentioning

confidence: 99%

Genetic risk factors for diabetic nephropathy on chromosomes 6p and 7q identified by the set-association approach

et al. 2007

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Aims/hypothesis In the present study we investigated potential associations of a set of 45 single nucleotide polymorphisms (SNP) in 20 candidate genes on eight chromosomes with diabetic nephropathy (DN) in type 2 diabetes mellitus. We aimed to compare two methodological approaches suitable for analysing susceptibility to complex traits: single-and multi-locus analyses. Materials and methods The study comprised a total of 647 subjects in one of three groups: diabetes with or without DN, or no diabetes. Genotypes were detected by PCRbased methodology (PCR only, PCR plus RFLP, or allelespecific PCR). Haplotypes were inferred in silico. Set association (tested using SUMSTAT software) was used for multilocus analysis.

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Section: Discussionmentioning

confidence: 99%

Genetic risk factors for diabetic nephropathy on chromosomes 6p and 7q identified by the set-association approach

et al. 2007

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“…19 NOS 3 polymorphisms associated with decreased NO production correlate with end-stage renal disease in humans. 20 These data suggest that lack of renal NO may be important in advanced nephropathy and renal damage. 21 In addition, promoting NO production by administering L-arginine is known to attenuate pregnancyinduced hypertension.…”

Section: Roles For Renal Nomentioning

confidence: 91%

Recent Advances in the Regulation of Nitric Oxide in the Kidney

Herrera

Garvin

2005

Hypertension

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Abstract-Nitric oxide (NO) plays important roles in the regulation of renal function and the long-term control of blood pressure. New roles of NO have been proposed recently in diabetes, nephrotoxicity, and pregnancy. NO derived from all 3 NOS isoforms contributes to the overall regulation of kidney function, and recent advances in our understanding of their regulation have been made lately. In this regard, substrate and cofactor availability play important roles in regulating nitric oxide synthase (NOS) activity not only by limiting enzyme activity but also by influencing the coupling of NOS with its cofactors, tetrahydrobiopterin and NADPH. Protein-protein interactions are now recognized to be important negative and positive regulators of NOS. Phosphorylation is another component of the mechanism whereby NOS is activated or deactivated. Increased NOS expression can also influence enzyme activity; however, the degree of expression does not always correlate with enzyme activity because increased NO levels can result in inhibition of NOS. Finally, other potential regulators of NOS such as endogenous L-arginine analogs may also be important. In this article, we summarize recent advances in the regulation of activity and expression of the NOS isoforms within the kidney. renal function and long-term regulation of blood pressure. [1][2][3][4] This is best evidenced by the fact that inhibiting intrarenal NO production increased blood pressure. 5 In addition, reduced NO has been identified as a common denominator of many hypertensive models. 6 -9 The effects of NO on blood pressure via actions in the kidney occur through multiple mechanisms. These include increasing renal blood flow caused by vasodilatation, 10 increasing glomerular filtration, 11 inhibiting sodium transport along the nephron, 12-14 and regulating release of renin. 15 NO produced by each of the 3 nitric oxide synthases (NOS), NOS 1, NOS 2, and NOS 3, reportedly contributes to the regulation of renal function. Inhibition of NOS activity within the kidney is known to lead to sodium retention and hypertension. This review addresses recent advances in our understanding of the role played by renal NO in various physiological and pathophysiological conditions, as well as how NO production is regulated. Roles for Renal NOHistorically, NO produced by the kidney has been thought of primarily as a factor that regulates urinary volume and sodium excretion. The physiological effects of NO can be mediated via changes in renal hemodynamics and/or salt and water absorption by the nephron. NO reduces renal vascular tone in part by dilating the afferent arteriole. 16 It also increases glomerular filtration rate. 11 NO modulates renin secretion by the juxtaglomerular apparatus 15 and tubuloglomerular feedback. 3 Finally, NO regulates transport in various nephron segments as reviewed recently by Ortiz and Garvin. 12 More recently it has been recognized that in a number of pathophysiological conditions, the actions of NO on renal hemodynamics and/or nephron transport are ...

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“…11 The relative contribution of these 2 mechanisms may be variable over time. It is suspected that functional hypoxia is the dominant factor early in the progression and oxidative stress may become dominant in the later stages.…”

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confidence: 99%

Early Changes With Diabetes in Renal Medullary Hemodynamics as Evaluated by Fiberoptic Probes and BOLD Magnetic Resonance Imaging

Santos

et al. 2007

Investigative Radiology

114

110

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Objective-We sought to evaluate the influence of streptozotocin (STZ)-induced diabetes on renal outer medullary pO 2 and blood flow by invasive microprobes and to demonstrate feasibility that blood oxygenation level-dependent (BOLD) magnetic resonance imaging (MRI) can monitor these changes.Materials and Methods-A total of 60 Wistar-Furth rats were used. Diabetes was induced by STZ in 48. Animals were divided into OxyLite group (n = 30) and BOLD MRI groups (n = 30) each with a 5 subgroups of 6 animals: control and 2, 5, 14, and 28 days after induction of diabetes. Outer renal medullary oxygen tension and blood flow were measured by the combined OxyLite/OxyFlo probes. Results-BothOxyLite and BOLD MRI showed a significant increase in the renal hypoxia levels after STZ at all time points. However, no changes were observed in the outer renal medullary oxygen tension and blood flow between diabetic and control groups.Conclusions-These preliminary results suggest that hypoxic changes can be detected as early as 2 days in rat kidneys with diabetes by BOLD MRI and that these early changes are not dependent on blood flow.

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Role of nitric oxide in diabetic nephropathy

Cited by 138 publications

References 86 publications

Genetic risk factors for diabetic nephropathy on chromosomes 6p and 7q identified by the set-association approach

Genetic risk factors for diabetic nephropathy on chromosomes 6p and 7q identified by the set-association approach

Recent Advances in the Regulation of Nitric Oxide in the Kidney

Early Changes With Diabetes in Renal Medullary Hemodynamics as Evaluated by Fiberoptic Probes and BOLD Magnetic Resonance Imaging

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